tbuckley/cabot-search huggingface dataset:
Hepatitis C viremia in chronic liver disease: Relationship to interferon-α or corticosteroid treatment
Authors: S Magrin
Journal: Hepatology (1994)

We assessed the pattern of hepatitis C viremia in chronic liver disease by studying 100 hepatitis C virus antibody–positive patients: 48 with chronic hepatitis, 21 with cirrhosis and 31 with hepatocellular carcinoma and cirrhosis. Serum hepatitis C virus RNA was detected by means of both the conventional nested polymerase chain reaction and a newly developed assay based on branched DNA that can also quantify viremia. Hepatitis C virus RNA was found in 94 of 100 patients with polymerase chain reaction and in 71 of 100 patients with branched-DNA (p < 0.001). Mean viremia level (× 103 genome equivalents/ml ± S.D.), as assessed with the branched-DNA test, was 5,700 ± 7,618 in the 48 patients with chronic hepatitis, 3,340 ± 3,633 in the 21 patients with cirrhosis and 1,768 ± 2,770 in the 31 patients with hepatocellular carcinoma (p < 0.02). We also analyzed retrospectively the relationship between viremia and treatment. Fifty-five patients (41 chronic hepatitis, 14 cirrhosis) underwent interferon-α treatment. Mean viremia level was comparable among the 30 responders (5,644 ± 8,207) and the 25 nonresponders (5,519 ± 6,208) to interferon, but it was significantly lower (1,841 ± 1,864) in the 12 of 30 responders (11 chronic hepatitis, 1 cirrhosis) who maintained remission up to 1 yr after cessation of interferon treatment. Fourteen patients (7 chronic hepatitis, 7 cirrhosis) with autoantibodies (12 antinuclear, 2 anti–liver-kidney microsomal) were treated with prednisone. The mean viremia level significantly increased after 3 mo of treatment, even in face of ALT decrease. In conclusion, serum hepatitis C virus RNA is detectable in almost all patients with hepatitis C virus antibody–positive chronic liver disease, polymerase chain reaction being more sensitive than the branched-DNA test. Hepatitis C viremia is lowest in patients with advanced liver disease. A low pretreatment value of viremia could identify patients with chronic hepatitis who will derive long-term benefit from interferon. Corticosteroids generally increase viremia in hepatitis C virus antibody–positive, autoantibody-positive chronic hepatitis, independent of ALT response. (Hepatology 1994;19:273–279).
Half-Life of Polybrominated Biphenyl in Human Sera
Authors: Daniel H. Rosen, W. Dana Flanders, Andrew Friede, Harold E. B. Humphrey, Thomas H. Sinks
Journal: Environmental Health Perspectives (1995)

Polybrominated biphenyl (PBB), a flame-retardant material, was introduced into the food chain in Michigan in 1973 due to a manufacturing and distribution mistake. Following public concern about the long-term health effects of PBB in humans, a cohort of PBB-exposed Michigan residents was assembled in 1975. We initiated this study to determine the half-life of PBB in human sera and to understand how continued body burden relates to the possible adverse health consequences of PBB exposure. To determine the half-life, eligible persons were selected from the cohort if they had at least two PBB measurements 1 year apart and had an initial level > or = 20 pbb. There were 163 persons who met the criteria with a median PBB level of 45.5 ppb. The estimated half-life is 10.8 years (95% CI, 9.2-14.7 years). The body burden of PBB in exposed persons will decrease only gradually over time. For persons with an initial level of 45.5 ppb of PBB, it will take more than 60 years for their PBB levels to fall below the current level of detection of 1 ppb.
Abstract 1123: Bcl-xL promotes metastasis via a novel nuclear function
Authors: Tiantian Zhang, Sha Li, Joseph Na, Soyoung Chi, George Zhang, Yi-Chieh Nancy Du
Journal: Cancer Research (2019)

Abstract Cancer cells often evade apoptosis through upregulation of anti-apoptotic proteins and/or downregulation of pro-apoptotic proteins. Bcl-xL, a negative regulator of mitochondria-mediated apoptosis, is frequently overexpressed in cancer cells. Bcl-xL has long been known for its function in regulating apoptosis during embryonic development and in pathological conditions. Any role that Bcl-xL might play in tumor metastasis has been ascribed to its anti-apoptotic function; i.e. Bcl-xL may increase metastasis by lending survival advantage to the tumor cells during the course of metastasis. However, we have demonstrated that Bcl-xL’s metastatic function is independent of its canonical anti-apoptotic activity and instead requires a novel nuclear function in cancer. We found that Bcl-xL promotes migration, even when cells are defective in mitochondria-mediated apoptosis. Consistently, Bcl-xL mutants lacking anti-apoptotic activity can still promote migration, induce epithelial-mesenchymal transition (EMT), upregulate TGFβ, and increase migration and invasion of pancreatic neuroendocrine tumor cells and breast cancer cells. Importantly, our data demonstrated that forcible localization of Bcl-xL outside the nucleus impairs its metastatic function. As a mitochondrial membrane protein in healthy cells, Bcl-xL’s transmembrane domain prevents its nuclear import. This suggests that Bcl-xL enters the nucleus by an active nuclear transport. We hypothesized that unique transporters likely exist so as to transport this normally mitochondria membrane-bound Bcl-xL protein to the nucleus. By using immunoprecipitation in combination with mass spectrometry, we identified a novel interacting partner of Bcl-xL. We are investigating whether this protein transports Bcl-xL into the nucleus to promote metastasis. Citation Format: Tiantian Zhang, Sha Li, Joseph Na, Soyoung Chi, George Zhang, Yi-Chieh Nancy Du. Bcl-xL promotes metastasis via a novel nuclear function [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 1123.
Ventilation Strategies for Acute Lung Injury and Acute Respiratory Distress Syndrome
Authors: Yuji Oba
Journal: JAMA (2008)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Laser Myomectomy
Journal: JAMA (1988)

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The Changing Etiology of Liver Abscess
Authors: Luis M. de la Maza
Journal: JAMA (1974)

The incidence of liver abscess discovered at autopsy at the Mallory Institute of Pathology has remained fairly constant over the past 70 years (0.57%). The causes, however, are changing. In a review of cases over the period 1959 through 1968, it was discovered that (1) the incidence of liver abscess secondary to acute appendicitis decreased, but liver abscess secondary to biliary obstruction from cholelithiasis or carcinoma increased, and (2) the percentage of abscesses associated with Gramnegative bacteria has increased steadily since the introduction of antibiotics.
THE DANCE OF DEATH
Journal: JAMA (1961)

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Animals in research
Authors: Sara Katherine Katz
Journal: JAMA (1989)

<h3>To the Editor.—</h3> Animals have proved to be invaluable in medical research and have benefited the welfare of both humans and animals.<sup>1</sup>However, "to protect animals from unnecessary pain"<sup>1</sup>and to simplify our understanding of some complex pathogenetic mechanisms, rational exploration of alternative models is warranted.<sup>2</sup> Dysfunctional human cilia produce considerable respiratory and other illnesses.<sup>3-5</sup>The animal model most often employed to study the problem, the mammalian tracheal explant, has yielded important information about this category of diseases. Noting that the cilia of<i>Tetrahymena pyriformis</i>are morphologically and functionally indistinguishable from those of humans,<sup>5,6</sup>I began, in high school, to culture this protozoa under varied conditions. My aim was to develop a simple, inexpensive protozoan model to study abnormal cilia. <h3>Study. —</h3> <i>Tetrahymena pyriformis</i>was cultured under baseline conditions at 25°C in proteose peptone broth (group I: control group) and in chemically altered environments (group
Archives of Surgery, Chicago
Journal: JAMA (1965)

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Prevention of Rh-haemolytic disease: results of the clinical trial. A combined study from centres in England and Baltimore.
Authors: C Clarke, W Donohoe, Catherine Durkin, R Finn, F Path, R Mcconnell, P Sheppard, D Phil, Shona Towers, J Woodrow, C Sheffield, Bradford Leeds, Janet Shaw, R Speight, L Tovey, Wilma Baltimore, J Bias, Jeanette Krevans, A Light-Orr
Journal: BMJ (1966)

Finn (1960), in Liverpool, first put forward the idea that it might be possible to prevent immunization of Rh-negative mothers by giving them antibody to destroy Rh-positive foetal cells.The suggestion derived from our earlier work on ABO incompatibility in relation to Rh immunization (Clarke et al., 1958), and the progress of the research since then has been described in four main papers.In the first two (Finn et al., 1961 ; Clarke et al., 1963) we described experiments which were successful in preventing Rh immunization in Rh-negative male volunteers.The basis of the procedure was to remove rapidly from the circulation previously injected chromium-tagged Rh- positive red cells by giving high-titre anti-D as an infusion of plasma.Later Gorman et al. (1963) (see also Freda and Gorman, 1962; Freda et al., 1964) suggested the use of anti-D gamma-globulin instead of plasma, and since then we have used gamma-globulin.In our third paper (Woodrow et al., 1965) we showed that injected Rh-positive foetal cells could be cleared from the cir- culation of Rh-negative women volunteers as effectively as the Rh-positive adult cells were cleared from the Rh-negative men.We also produced evidence to show that the majority of cases of appreciable transplacental haemorrhage occurred during labour or very shortly before it, and, moreover, the greater the number of foetal cells found after delivery the greater was the likelihood of subsequent immunization.In this third paper we also stated that we had begun a clinical trial, in collaboration with colleagues working in Sheffield, Leeds, Bradford, and Baltimore, and the preliminary results of this were reported in August of last year (Clarke and Sheppard, 1965).Subsequently we described experiments which indicated that 1 ml. of gamma- globulin might be as effective in giving protection against the development of antibodies as the 5 ml.which we had used up to then (Clarke et al., 1966).In the present paper we describe the clinical trial, which has demonstrated that, anyhow up to six months after delivery, the technique which was successful in protecting against experi- mental Rh immunization has also protected women from Rh immunization by their Rh-positive foetuses.
Torch &amp;amp; Crucible: The Life and Death of Antoine Lavoisier
Journal: JAMA (1941)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Felty's syndrome.
Journal: BMJ (1971)

Despite the ample collateral circulation treatment has been directed towards the operative relief of the coeliac stenosis.Most authorsl 3 4 consider that removal of the compressive agent is adequate, but R. S. A. Lord and colleagues5 think that the artery is so damaged as to make its excision and reconstruction mandatory.Othersl 4 have angiographic proof that residual stenosis will resolve after the compressive agent has been removed and are therefore opposed to this extreme view.Disagreement exists on whether compression is due to the median arcuate ligament of the diaphragm3 or fibrosis in the coeliac plexus or ganglion.&8This is an important distinction, for it allows explanation of the syndrome either on rheological or on neurological grounds.Possibly the coeliac nervous plexus give rises to, or transmits, the pain, and the success of the operation depends more on neurec- tomy than arterial decompression.4 8 The success of surgical treatment varies in the different reports, ranging from 100%1 8 to 40%.4If the 72 cases whose follow-up has been reported may be considered as one group, then 79% were rendered asymptomatic, 11% improved, and 10% unaltered by operation.For the 53 cases from North America alone the figures are 88%, 8%, and 4%, while those from Europe are 63%, 16%, and 21%.Such therefore are the difficulties in understanding the coeliac axis compression syndrome that its existence and definition ought still to be considered sub judice, and patients should be exposed to the risks of angiography and surgical treatment only after the utmost circumspection.In the meantime every opportunity should be taken to document the visceral circulation in health and disease to improve our understanding of the role of ischaemia as a cause of gastroenterological symptoms.
Fissure of the anus and Fistula in Ano.
Journal: JAMA (1893)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
FOR REVENUE ONLY.
Journal: JAMA (1995)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Gastric Cancer and Lymphoma
Authors: H Pylori Triglyceride, Vivo Ma, Asante Ha, P Patel, J Levy, R Lloyd, C Finlayson, M Mendall, Peptic Ulceration, S Peek, J Thompson, M Atherton, G Blaser
Journal: Gut (1995)

Background: The pathogenic mechanisms by which H.pylori induces gastritis and peptic ulcer disease are unclear.In vitro studies suggest that H. pylori produces several enzymes including triglyceride lipase which may contribute to pathogenesis'.It has been postulated that triglyceride lipase hydrolyses mucus triglycerides resulting in a weaker mucus gel thus making the underlying mucosa more susceptible to acid/peptic attack.However the effect on gastric mucus by this enzyrne in vivo has not been investigated.Aim: To investigate the effect of H.pylori triglyceride lipase on gastric mucus in vivo.Methods: 23 H. pylon positive (mean age: 47yr, range 27-70, m:f 13:10) and 19 H. pylori negative (mean age: 46yr, range 23-64, m:f 9:10) dyspeptic patients attending for endoscopy were recruited.At endoscopy 3 antral biopsies were taken; 1 for biopsy urease test and 2 for histological assessment of H. pylon infection density (graded 0-3).Antral surface mucus was obtained with a cytology brush and total glycerol fatty acid esters measured colorimetrically after homogenisation.Total glycerides were extracted by the Folch technique and mono, di and triglycerides species separated on TLC.Bands were visualised with iodine vapour and sulphuric acid charring.Results: Mucus from H. pylon positive patients had a mean (SE) triglyceride of 27.1(7.6)nmollmg protein compared with 8.4(3.1)nmollmg protein (p<0.05) for H. pylon negative patients.There was no correlation between mucus triglyceride and the degree of mucosal inflammation assessed by mucosal neutrophil infiltration scores (Rs= .32,p= 0.12).TLC analysis of glycerides showed no lipolytic activity by the absence of bands corresponding with breakdown product of triglycerides (mono-and diglycerides).Conclusions: There is no significant H. pylon triglyceride lipase activity against mucus in vivo suggesting that this is not important in pathogenesis of peptic ulcer and gastritis.H.pylori infection increases the triglyceride content in mucus but the mechanism and significance of this are not clear from this study.